IMPAIRED GUT LIPID ABSORPTIVE-CAPACITY AFTER TRAUMA-HEMORRHAGE AND RESUSCITATION

Although the barrier function of the intestinal mucosa is impaired aft er hemorrhage, it remains unclear whether this is associated with a de ficit in mucosal function. The aim of this study, therefore, was to de termine whether trauma-hemorrhage affects the in vivo lipid absorptive capacity of the gut and, if so, to characterize the uptake process of free fatty acids in isolated enterocytes. To study this, rats were an esthetized, a laparotomy was performed (i.e., trauma was induced), and various blood vessels were cannulated. For in vivo lipid absorption, the main intestinal lymph vessel was cannulated and a jejunostomy feed ing tube was inserted. The animals were bled to and maintained at a me an arterial pressure of 40 mmHg until 40% of shed blood volume was ret urned in the form of Ringer lactate. They were then resuscitated with four times the volume of maximal bleed out with Ringer lactate. The in vivo and in vitro lipid absorptive capacities were assessed by measur ing lymph triglyceride output after a fat load and by determining the linoleic acid uptake rates on isolated enterocytes, respectively. The results show that the in vivo lipid absorption capacity of the gut is severely depressed after trauma-hemorrhage and resuscitation. Similarl y, in enterocytes isolated from hemorrhaged rats, fatty acid uptake ca pacity, as reflected by the decreased maximal uptake rates, was signif icantly reduced: 1.2 +/- 0.2 and 2.6 +/- 0.6 nmol . min(-1). 10(6) cel ls(-1) for hemorrhaged and sham, respectively. Thus gut lipid absorpti ve function is depressed after trauma-hemorrhage and resuscitation, wh ich is at least partially due to the depressed uptake mechanism of the enterocyte.